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anti-Human Retinoblastoma Binding Protein 8 Antikörper:
anti-Mouse (Murine) Retinoblastoma Binding Protein 8 Antikörper:
anti-Rat (Rattus) Retinoblastoma Binding Protein 8 Antikörper:
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Human Monoclonal Retinoblastoma Binding Protein 8 Primary Antibody für ICC, IF - ABIN2668263
Zhou, Caron, Legube, Paull: Quantitation of DNA double-strand break resection intermediates in human cells. in Nucleic acids research 2014
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Human Polyclonal Retinoblastoma Binding Protein 8 Primary Antibody für ICC, IF - ABIN256682
Quennet, Beucher, Barton, Takeda, Löbrich: CtIP and MRN promote non-homologous end-joining of etoposide-induced DNA double-strand breaks in G1. in Nucleic acids research 2011
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Human Monoclonal Retinoblastoma Binding Protein 8 Primary Antibody für ChIP, ICC - ABIN445506
Liu, Lee: CtIP activates its own and cyclin D1 promoters via the E2F/RB pathway during G1/S progression. in Molecular and cellular biology 2006
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Human Polyclonal Retinoblastoma Binding Protein 8 Primary Antibody für IP - ABIN256681
Yin, Seifert, Chua, Maure, Golebiowski, Hay: SUMO-targeted ubiquitin E3 ligase RNF4 is required for the response of human cells to DNA damage. in Genes & development 2012
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53BP1 (zeige TP53BP1 Antikörper)/RIF1 (zeige INSL6 Antikörper) has a role in limiting BRCA1/CtIP-mediated end resection to control double strand break repair pathway choice
we reveal that reprogramming is associated with high levels of DNA end resection, a critical step in homologous recombination. Moreover, the resection factor CtIP is essential for cell reprogramming and establishment of iPSCs, probably to repair reprogramming-induced DNA damage.
Data show that SUMO E3 ligase (zeige PIAS1 Antikörper) CBX4 (zeige CBX4 Antikörper) sumoylates subpopulation of CtIP to regulate recruitment to breaks and resection.
CtIP/Ctp1/Sae2/Com1 role in removal of DNA double strand breaks through DSB repair by homologous recombination is reviewed.
Data delineates the regulatory mechanisms of GATA3 (zeige GATA3 Antikörper) in DNA double-strand breaks repair and strongly suggests that it might act as a tumor suppressor by promoting CtIP expression and homologous recombination to stabilize genomes.
The results illuminate the important role of Nbs1 (zeige NBN Antikörper) and CtIP in determining the substrates and consequences of human Mre11 (zeige MRE11A Antikörper)/Rad50 (zeige RAD50 Antikörper) nuclease (zeige DCLRE1C Antikörper) activities on protein-DNA lesions.
And-1 interacts with CtIP and that these interactions are required for DNA damage checkpoint maintenance, thereby linking DNA processing with prolonged cell cycle arrest to allow sufficient time for DNA repair.
his shows that 53BP1 (zeige TP53BP1 Antikörper) protects both close and distant DSEs from degradation and that the association of unprotection with distance between DSEs favors ECS capture. Reciprocally, silencing CtIP lessens ECS capture both in control and 53BP1 (zeige TP53BP1 Antikörper)-depleted cells. We propose that close ends are immediately/rapidly tethered and ligated, whereas distant ends first require synapsis of the distant DSEs prior to ligation
Low level of CtIP expression is associated with breast cancer.
Homozygous RBBP8 mutation is associated with microcephaly, intellectual disability, short stature and brachydactyly.
CtIP is not a tumor suppressor, but has oncogenic properties that can promote tumorigenesis, consistent with its ability to facilitate MMEJ-dependent chromosomal instability.
Q418P nsSNP influences the efficiency of CTIP function in HR repair of DNA DSBs
Ctip1 (zeige BCL11A Antikörper) couples subtype and area specification, enabling specific functional areas to organize precise ratios of appropriate output projections.
work therefore ascribes novel roles for BRCA1 (zeige BRCA1 Antikörper) and CtIP in end-processing and fusion reactions at uncapped telomeres
Data indicate that loss of the CtIP-BRCA1 interaction does not detectably affect resection, maintenance of genomic stability or viability.
The phospho-dependent BRCA1 (zeige BRCA1 Antikörper)-CtIP interaction is not essential for HDR (zeige GATA3 Antikörper)-mediated DSB repair or for tumor suppression.
CtIP contributes to the metabolism of DNA ends during DNA double-strand breaks repair in B lymphocytes.
CtIP-mediated alt-NHEJ has a primary role in translocation formation.
CtIP binds to switch-region DNA and plays a physiological role in microhomology-mediated end joining in a C-NHEJ-proficient environment.
MRN (Mre11 (zeige MRE11A Antikörper), Rad50 (zeige RAD50 Antikörper), and Nbs1 (zeige NLRP2 Antikörper)) complex, CtIP, and BRCA1 are required for both the removal of Top2 (zeige TOP2 Antikörper)-DNA adducts and the subsequent resection of Top2 (zeige TOP2 Antikörper)-adducted DSB ends.
ATM (zeige ATM Antikörper) activity is required for an early step in resection, leading to ATR (zeige ATR Antikörper) activation, CtIP-T818 phosphorylation, and accumulation of CtIP on chromatin.
By promoting CtIP-dependent resection of double-strand break (DSB) ends while preventing Rad51 chromatin assembly, Cdk1 (zeige CDK1 Antikörper) inhibits both the nonhomologous and homologous modes of DSB repair during mitosis.
The protein encoded by this gene is a ubiquitously expressed nuclear protein. It is found among several proteins that bind directly to retinoblastoma protein, which regulates cell proliferation. This protein complexes with transcriptional co-repressor CTBP. It is also associated with BRCA1 and is thought to modulate the functions of BRCA1 in transcriptional regulation, DNA repair, and/or cell cycle checkpoint control. It is suggested that this gene may itself be a tumor suppressor acting in the same pathway as BRCA1. Three transcript variants encoding two different isoforms have been found for this gene. More transcript variants exist, but their full-length natures have not been determined.
, DNA endonuclease RBBP8
, sporulation in the absence of SPO11 protein 2 homolog
, ctBP-interacting protein
, retinoblastoma-binding protein 8
, retinoblastoma binding protein 8
, CtBP-interacting protein
, retinoblastoma-binding protein 8-like